The infusion of funds from the Greenebaum family will predominantly support pioneering faculty research at the University of Maryland School of Medicine (UMSOM), bolstering efforts to develop cutting-edge cancer therapies. A major focus will be on immunotherapies, particularly chimeric antigen receptor (CAR) T-cell therapies, which have revolutionized treatment paradigms in hematologic malignancies and are now being explored aggressively for efficacy against solid tumors. This strategy involves reprogramming a patient’s immune cells to recognize and eradicate cancer cells with heightened specificity, offering hope for treating cancers that have historically been resistant to conventional approaches.

Beyond therapeutic innovations, the endowment will also strengthen survivorship programs at UMGCCC. Emerging wearable technologies capable of continuous physiological monitoring will be integrated into patient care strategies to optimize quality of life for cancer survivors. Personalized supportive care, including tailored nutritional regimens and psychosocial resources, will form a crucial component in enhancing long-term outcomes and mitigating treatment-related toxicities. This holistic approach underscores the center’s commitment to not only prolong lives but also improve the lived experience of patients beyond their clinical treatment.

As UMGCCC prepares for a significant physical expansion with its relocation to the Stoler Center for Advanced Medicine scheduled for fall 2026, the family’s donation assumes added significance. The new facility’s lobby will bear the Greenebaum name, symbolizing their enduring impact on the institution. The Stoler Center will house state-of-the-art laboratories, patient care suites, and clinical trial infrastructure designed to facilitate seamless translational research and multidisciplinary collaboration, ultimately accelerating the bench-to-bedside delivery of novel therapies.

Michael Greenebaum, scion of the Greenebaum family and an influential philanthropist, articulated the familial dedication behind the gift. Marking the 30th anniversary of the original donation, he emphasized that the contribution empowers the center to meet the escalating demand for expert oncology care in Maryland and its surrounding regions. The family’s longstanding involvement exemplifies how philanthropy can catalyze scientific breakthroughs and foster comprehensive patient-centric cancer care.

The Greenebaum family’s involvement extends beyond financial support. Michael Greenebaum serves as Chair of the University of Maryland School of Medicine’s Board of Visitors and sits on the UMGCCC Board of Advisors. He is also the founder of the Maryland Half-Marathon & 5K, which has raised over $8 million for the center, demonstrating an innovative approach to community engagement in cancer fundraising. This multi-faceted participation underscores the synergistic relationship between leadership, philanthropy, and research advancement.

The foundational success story of Marlene Greenebaum’s battle with breast cancer is intertwined with pioneering research at UMGCCC. She benefited from treatment with an aromatase inhibitor, a type of hormone therapy developed by Angela Brodie, PhD, a leading breast cancer researcher associated with the cancer center. Aromatase inhibitors function by blocking the enzyme aromatase, which converts androgens to estrogens, thereby reducing estrogen levels that fuel hormone receptor-positive breast cancers. This therapeutic breakthrough has become a standard of care globally, emblematic of how translational science at academic centers can alter clinical practices.

Leadership at UMGCCC recognizes the critical importance of sustained philanthropic support. Dr. Taofeek K. Owonikoko, the center’s Executive Director, noted that continuous funding is imperative for maintaining the momentum of clinical trials, which now number over 450 and represent a doubling from earlier years. These trials explore next-generation agents, combination immunotherapies, precision oncology approaches, and modalities aimed at overcoming tumor microenvironment-mediated resistance pathways. Such a robust clinical pipeline positions the center as a leader in oncology innovation.

UMGCCC’s research budget exceeds $130 million annually, reflecting its stature as a premier academic and research institution. The breadth of oncology clinical and basic research encompasses molecular biology, genomics, immunology, bioinformatics, and population health studies. The center’s faculty conduct extensive investigations into tumor biology, mechanisms of metastasis, and the development of novel biomarkers to enable early detection and therapeutic responsiveness. This comprehensive research spectrum embodies a systems biology approach to conquering cancer’s complexity.

The clinical environment benefits enormously from integration with UMGCCC’s basic science enterprises. The reciprocal relationship facilitates rapid hypothesis testing and functional validation of emerging targets in vivo through patient-derived xenograft models and organoid cultures. Moreover, the multidisciplinary teams comprising oncologists, surgeons, radiologists, pathologists, and data scientists collaborate intensively to tailor individualized treatment regimens, reinforcing the precision medicine paradigm.

Maryland’s University of Maryland Medical Center (UMMC), the flagship hospital in the 11-hospital University of Maryland Medical System (UMMS), serves as the clinical anchor for UMGCCC. UMMC’s advanced infrastructure supports high-complexity procedures, including solid organ transplantation and sophisticated imaging modalities vital for cancer diagnosis and management. The integration of clinical care and research fosters an ecosystem that translates scientific discoveries swiftly into standard practice, benefiting thousands of patients annually.

The upcoming expansion into the Stoler Center also represents a strategic bet on the future of oncology, emphasizing seamless integration of digital health technologies, telemedicine capabilities, and patient navigation services to improve access and adherence to cancer care protocols. The center’s mission aligns with global efforts to reduce cancer mortality through innovation while addressing survivorship challenges in an aging population that increasingly confronts late effects of cancer treatment.

In conclusion, the recent $5.5 million gift from the Marlene and Stewart Greenebaum Family Foundation marks a significant milestone for the University of Maryland Greenebaum Comprehensive Cancer Center. This philanthropic investment supports transformative cancer research, accelerates development of breakthrough therapies like CAR T-cell treatment for solid tumors, and enhances survivorship programs through advanced wearable technologies and tailored clinical support. The planned move to the Stoler Center for Advanced Medicine will bolster these efforts, situating UMGCCC to remain at the vanguard of cancer care and research. The Greenebaum family’s enduring legacy continues to inspire scientific innovation and exceptional patient care, reaffirming the profound impact of philanthropy in advancing the fight against cancer.

Subject of Research: Cancer research and treatment innovations at the University of Maryland Greenebaum Comprehensive Cancer Center, including immunotherapies and survivorship care.

Article Title: University of Maryland Greenebaum Comprehensive Cancer Center Receives $5.5 Million Gift to Accelerate Cancer Research and Care Expansion

News Publication Date: Not specified in the source content.

Web References:

• https://www.umms.org/umgccc
• https://www.umms.org/about/leadership/mohan-suntha
• https://www.medschool.umaryland.edu/profiles/gladwin-mark/
• https://www.umms.org/ummc/about/leadership/bert-w-omalley
• https://www.umms.org/find-a-doctor/profiles/dr-taofeek-kunle-owonikoko-md–phd-1578770871
• https://www.umms.org/ummc/about/leadership/heather-culp
• https://www.medschool.umaryland.edu/
• http://www.umm.edu/
• http://www.umms.org/

Image Credits: University of Maryland School of Medicine

Keywords: Cancer research, Immunotherapy, CAR T-cells, Survivorship care, Philanthropy, University of Maryland Greenebaum Comprehensive Cancer Center, Translational medicine, Clinical trials, Oncology innovation, Comprehensive cancer center

While CAR T-cell therapy has revolutionized treatment for certain blood cancers, its application to solid tumors has faced significant challenges due to the hostile, immunosuppressive microenvironment these tumors create. PGE2, a bioactive lipid mediator prevalent in the tumor milieu, plays a pivotal role in dampening immune responses by engaging its receptors on immune cells, effectively muffling the anti-tumor activity of CAR T cells. Recognizing this, the research team embarked on a meticulous genetic engineering approach to disable both major PGE2 receptors on CAR T cells, thereby liberating them from this inhibitory cascade.

The dual receptor knockout was engineered using state-of-the-art gene editing tools that ensure both accuracy and durability of receptor ablation within the CAR T-cell genome. This precise gene editing approach was followed by rigorous functional assays to confirm that the modified CAR T cells were not only free from PGE2-mediated signaling but also retained their vital cytotoxic functions and proliferative capacity. Strikingly, these reprogrammed immune cells exhibited a marked resistance to the immunosuppressive forces typically present in the tumor microenvironment.

In preclinical models of notoriously resistant solid tumors, the modified CAR T cells demonstrated a significantly enhanced ability to infiltrate tumor masses and sustain their anti-cancer activity over extended periods. This translated into a profound delay in tumor progression and, in some cases, complete regression, effects seldom seen with conventional CAR T therapies. The results suggest that by cutting off PGE2 signaling at the receptor level, CAR T cells can overcome one of the critical molecular brakes imposed by solid tumors.

Beyond their improved efficacy, these receptor-deficient CAR T cells also showed a surprising reduction in systemic inflammatory side effects, a common complication of cellular immunotherapies. This suggests not only a better therapeutic index but also raises hopes for improved patient tolerability and safety profiles in eventual clinical applications. The dual receptor ablation may thus represent a critical balancing act, enhancing tumor targeting while mitigating collateral immune activation.

The strategy emerges from an extensive understanding of PGE2’s multifaceted role in tumor biology and immune evasion. By disabling two distinct receptors, the approach assures a more comprehensive blockade of PGE2’s immunosuppressive signals, which might otherwise bypass single receptor-targeted interventions. This dual knockout thus reflects a sophisticated approach to target redundancy and compensatory pathways that cancers often exploit.

Importantly, the research also addressed concerns about potential alterations in CAR T-cell homing and survival mechanisms due to receptor ablation. Detailed phenotypic analyses revealed that the dual receptor knockout did not impair essential receptor signaling pathways responsible for normal T-cell function and navigation, preserving the therapeutic cells’ fitness and resilience in vivo.

Further in-depth molecular profiling illuminated how disabling PGE2 receptors recalibrates the CAR T-cell transcriptome towards a more activated and persistent state, characterized by upregulation of effector molecules and resistance to exhaustion, a chronic dysfunction state that often limits CAR T efficacy. These gene expression changes resonate with improved functional outputs observed upon tumor challenge.

The translational implications of these findings cannot be overstated. By providing a robust methodology to empower CAR T cells against formidable solid tumor defenses, this research paves the way for new clinical trials aiming to extend CAR T-cell therapy beyond hematological malignancies. It also highlights the potential of combinatorial genetic targeting strategies to overcome intrinsic tumor immune resistance.

Moreover, these advances may open doors for integrating dual PGE2 receptor deletion with other CAR T modifications such as co-stimulatory domain optimization or checkpoint blockade to create next-generation cellular therapies that synergize multiple mechanisms for maximal eradication of solid tumors.

While further studies are warranted to assess long-term efficacy, safety, and potential off-target effects in humans, this seminal work lays a critical foundation for future CAR T-cell engineering. It signals a significant leap towards harnessing the full therapeutic potential of cellular immunotherapies against the stubborn challenge posed by solid cancers.

The successful application of dual receptor knockout in this context also invigorates interest in the broader field of tumor microenvironment modulation. It underscores the importance of understanding and intervening in the complex signaling networks that tumors exploit to evade immune destruction.

Ultimately, this research exemplifies the fusion of molecular biology, immunotherapy, and gene editing technologies to surmount formidable clinical challenges. It heralds a promising era where engineered T cells can be fine-tuned with unprecedented precision to achieve durable, potent responses in patients battling solid tumors, a goal long sought but rarely realized in oncology.

As the scientific community eagerly watches the progression of these engineered cellular therapies into clinical settings, hopes are high that such innovations will translate to meaningful improvements in patient outcomes, offering renewed optimism in the relentless fight against cancer.

Subject of Research: Enhancing CAR T-cell therapy efficacy in solid tumors by genetically ablating prostaglandin E2 signaling through dual receptor knockout.

Article Title: Ablation of prostaglandin E2 signalling through dual receptor knockout in CAR T cells enhances therapeutic efficacy in solid tumours.

Article References:
Dörr, J., Gregor, L., Lacher, S.B. et al. Ablation of prostaglandin E2 signalling through dual receptor knockout in CAR T cells enhances therapeutic efficacy in solid tumours. Nat. Biomed. Eng (2026). https://doi.org/10.1038/s41551-025-01610-6

Image Credits: AI Generated

DOI: https://doi.org/10.1038/s41551-025-01610-6